MAA-epitopes are lipid peroxidation-derived danger signals that are sensed by macrophages and bound by the humoral innate immune defense protein FH. We hypothesize that MAA-epitopes represent effectors of lipotoxicity and that they are mediators of inflammation in various pathologies, including atherosclerosis. Thus, we aim to elucidate the consequences of defective lipolysis on innate immune responses in macrophages in vitro and murine models in vivo, and assess the contribution of MAA-epitopes to these responses. We will define the cellular responses of macrophages sensing MAA-epitopes, and the protective capacity of FH-mediated scavenging will be studied in murine atherosclerosis.